The pain of migraine headaches might not be caused by expanded blood vessels in the brain, as previously thought. Instead, the real culprit may be overactive pain-signal firing in brain cells, new research suggests.
Moreover, there are several treatments being developed that could address this signaling and, in turn, help treat migraine pain. However, further studies are needed to confirm that the overactive signaling is a cause of migraine pain.
"Many people are nonresponders to existing drugs," said study co-author Dr. Messoud Ashina, a physician at the University of Copenhagen in Denmark. "So there is room for improvement — that's why we need the new drugs."
Ashina and his co-authors have received money from pharmaceutical companies.The findings, which were published online April 9 in the journal Lancet Neurology, come from studying the brain scans of patients as they were suffering from a migraine.
About one in 10 Americans suffer from migraines, with women more likely to be affected. The headaches typically last from four to 72 hours, and are often accompanied by nausea, pain, and sensitivity to light and sound. Past studies showed an increased risk of stroke and depression in women who suffer from migraines.
The most common treatments for migraines, a class of medicines called triptans, were thought to relieve migraine pain by constricting blood vessels in the brain. But past research suggested only 30 percent of people suffering from a migraine are pain-free two hours after taking a triptan, Ashina said.
In recent decades, researchers have wondered whether pain signals from sensory neurons in the brain may be the true cause of migraine pain.
To study migraines in real time, Ashina and his colleagues looked at 19 women who were experiencing migraines. Using a technique called magnetic resonance angiography, the scientists measured the blood flow in the women's brains, and found that only a few blood vessels inside the brain were modestly dilated.
Then, they gave patients a triptan, and their average pain levels reduced dramatically.
However, the triptans constricted blood vessels on the outside of the brain, not the vessels that were mildly dilated during the migraine. That suggests that the triptans relieved migraine pain not by constricting blood vessels, but by another mechanism — possibly by quieting pain signals from neurons.
The findings cast doubt on vessel dilation as the primary cause of migraine pain, Ashina said.
"We think that the pain signals are coming from the neurons, and the modest dilation that we see — it is a kind of consequence of this activation of these neurons," Ashina said.
That's good news, because several potential migraine treatments — which belong to a class of medicines called CGRP antagonists and are designed to specifically target the chemical signals implicated in migraine pain — are already being developed, Ashina said.
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